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  • 绿原酸

    Chlorogenic acid

    绿原酸
    产品编号 CFN99116
    CAS编号 327-97-9
    分子式 = 分子量 C16H18O9 = 354.31
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Phenylpropanoids
    植物来源 The barks of Eucommia ulmoides Oliv.
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    绿原酸 CFN99116 327-97-9 10mg QQ客服:2056216494
    绿原酸 CFN99116 327-97-9 20mg QQ客服:2056216494
    绿原酸 CFN99116 327-97-9 50mg QQ客服:2056216494
    绿原酸 CFN99116 327-97-9 100mg QQ客服:2056216494
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • Fraunhofer-Institut für Molekularbiologie und Angewandte ?kologie IME (Germany)
  • Universiti Kebangsaan Malaysia (Malaysia)
  • John Innes Centre (United Kingdom)
  • University of Liège (Belgium)
  • Korea Intitute of Science and Technology (KIST) (Korea)
  • Universiti Malaysia Pahang (Malaysia)
  • Monash University Malaysia (Malaysia)
  • Semmelweis Unicersity (Hungary)
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  • University of Amsterdam (Netherlands)
  • University of Toronto (Canada)
  • Kyushu University (Japan)
  • The University of Newcastle (Australia)
  • Universidade Federal de Goias (UFG) (Brazil)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Front Microbiol.2022, 12:833233.
  • Food Structure2023, 36:100324.
  • In Vivo.2022, 36(3):1136-1143.
  • J Appl Biol Chem2021, 64(3):245-251.
  • Front Microbiol.2023, 14:1232039.
  • Green Chemistry2021, ISSUE 2.
  • Sci Rep.2019, 9:19059
  • J Pharm Biomed Anal.2018, 151:32-41
  • Curr Issues Mol Biol.2022, 44(5):2300-2308.
  • Journal of Phytopathology2021, 169,Issue11-12.
  • Molecules.2019, 24(11):E2102
  • Molecules 2022, 27(3),1047.
  • Korean J of Pharmacognosy2020, 51,49-54.
  • Biol Pharm Bull.2021, 44(12):1891-1893.
  • Food Chem.2021, 337:128023.
  • Chem Biodivers.2023, 20(10):e202300741.
  • Theoretical and Experimental Plant Physiology 2022, 34,53-62
  • PLoS One.2017, 12(3):e0173585
  • Korean Journal of Pharmacognosy2018, 49(1):76-83
  • Naunyn Schmiedebergs Arch Pharmacol.2017, 390(10):1073-1083
  • Phytother Res.2022, 10.1002:ptr.7626.
  • J Drug Target.2016, 24:1-28
  • Food Research International2016, 106-113
  • ...
  • 生物活性
    Description: Chlorogenic acid, a phenolic compound found ubiquitously in plants, is an antioxidant and metal chelator, it has antiviral activity by inhibiting HBV replication, it inhibits the inflammatory reaction in HSE via the suppression of TLR2/TLR9-Myd88 signaling pathways. Some derivatives of chlorogenic acid are hypoglycemic agents and may affect lipid metabolism, chlorogenic acid can improve glucose tolerance, decrease some plasma and liver lipids, and improve mineral pool distribution in vivo.
    Targets: HBV | PEG | NO | NOS | ERK | ROS | COX
    In vitro:
    Anticancer Drugs. 2015 Feb 24.
    Chlorogenic acid enhances the effects of 5-fluorouracil in human hepatocellular carcinoma cells through the inhibition of extracellular signal-regulated kinases.[Pubmed: 25714249]
    There is an urgent need to search for novel chemosensitizers in the field of cancer therapy. Chlorogenic acid (CGA), a type of polyphenol present in the diet, has many biological activities.
    METHODS AND RESULTS:
    The present study is designed to explore the influence of CGA on the effects of 5-fluorouracil (5-FU) on human hepatocellular carcinoma cells (HepG2 and Hep3B). Treatment with 5-FU induced the inhibition of hepatocellular carcinoma cells' proliferation, and the combined treatment with CGA enhanced this inhibition. 5-FU also increased the production of reactive oxygen species (ROS). The combination of 5-FU and CGA led to a more prominent production of ROS and significantly inactivated ERK1/2, although CGA and 5-FU exerted no significant changes when used alone. A previous report has shown that ROS are upstream mediators that inactivate ERK in hepatocellular carcinoma cells. Combined with our results, this indicates that the combination of 5-FU and CGA leads to the inactivation of ERK through the overproduction of ROS. This mediates the enhancement of 5-FU-induced inhibition of hepatocellular carcinoma cells' proliferation, that is, CGA sensitizes hepatocellular carcinoma cells to 5-FU treatment by the suppression of ERK activation through the overproduction of ROS.
    CONCLUSIONS:
    CGA has shown potential as a chemosensitizer of 5-FU chemotherapy in hepatocellular carcinoma.
    Cell Oncol (Dordr) . 2015 Apr;38(2):111-8.
    Chlorogenic acid inhibits hypoxia-induced angiogenesis via down-regulation of the HIF-1α/AKT pathway[Pubmed: 25561311]
    Background: The hypoxia-inducible factor-1 (HIF-1) is known to play an important role in cellular responses to hypoxia, including the transcriptional activation of a number of genes involved in tumor angiogenesis. Chlorogenic acid (CGA), one of the most abundant polyphenols in the human diet, has been reported to inhibit cancer cell growth. The effect of CGA on tumor angiogenesis and its underlying mechanisms are, as yet, unknown. Methods: The effect of CGA on HIF-1α expression was assessed by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR) assays in A549 lung cancer cells. The transcriptional activity of the HIF-1 complex was confirmed using a luciferase assay. To assess whether angiogenic factors are increased under hypoxic conditions in these cells, vascular endothelial growth factor (VEGF) expression levels were measured by RT-PCR and Western blotting. The direct effect of CGA on human vascular endothelial cells (HUVEC) under hypoxic conditions was analyzed using in vitro assays, including tube-formation, wound healing and Transwell invasion assays. To investigate the effect of CGA on angiogenesis in vivo, we performed a Matrigel plug assay in a mouse model. Finally, the effect of CGA on AKT and ERK activation (phosphorylation) as a putative mechanism underlying the effect of CGA on VEGF-mediated angiogenesis inhibition was assessed using Western blotting. Results: We found that CGA significantly decreases the hypoxia-induced HIF-1α protein level in A549 cells, without changing its mRNA level. CGA was, however, found to suppress the transcriptional activity of HIF-1α under hypoxic conditions, leading to a decrease in the expression of its downstream target VEGF. We also found that CGA can block hypoxia-stimulated angiogenesis in vitro and VEGF-stimulated angiogenesis in vivo using HUVEC cells. In addition, we found that CGA can inhibit the HIF-1α/AKT signaling pathway, which plays an important role in VEGF activation and angiogenesis. Conclusions: Our data indicate that CGA plays a role in the suppression of angiogenesis via inhibition of the HIF-1α/AKT pathway. CGA may represent a novel therapeutic option for the treatment of (lung) cancer.
    In vivo:
    Int J Pharm. 2011 Jan 17;403(1-2):136-8.
    In vitro and in vivo antioxidant properties of chlorogenic acid and caffeic acid.[Pubmed: 20933071 ]
    Dietary polyphenols are thought to be beneficial for human health as antioxidants. Coffee beans contain a common polyphenol, chlorogenic acid. Chlorogenic acid is the ester of caffeic acid and quinic acid. Although these polyphenols have received much attention, there is little evidence indicating a relationship between the effect and the rate of absorption.
    METHODS AND RESULTS:
    In this study, we focused on the beneficial effects of chlorogenic acid and caffeic acid, a major metabolite of chlorogenic acid. We carried out in vitro and in vivo experiments. In the in vitro study, caffeic acid had stronger antioxidant activity than that of chlorogenic acid. The uptake of chlorogenic acid by Caco-2 cells was much less than that of caffeic acid. The physiological importance of an orally administered compound depends on its availability for intestinal absorption and subsequent interaction with target tissues. We then used an intestinal ischemia-reperfusion model to evaluate antioxidant activities in vivo.
    CONCLUSIONS:
    We found that both chlorogenic acid and caffeic acid had effects on intestinal ischemia-reperfusion injury. Since caffeic acid has a stronger antioxidant activity than that of chlorogenic acid and chlorogenic acid is hydrolyzed into caffeic acid in the intestine, it is possible that caffeic acid plays a major role in the protective effect of chlorogenic acid against ischemia-reperfusion injury.
    J Nutr Biochem. 2002 Dec;13(12):717-726.
    Chlorogenic acid modifies plasma and liver concentrations of: cholesterol, triacylglycerol, and minerals in (fa/fa) Zucker rats.[Pubmed: 12550056]
    Chlorogenic acid, a phenolic compound found ubiquitously in plants, is an in vitro antioxidant and metal chelator. Some derivatives of chlorogenic acid are hypoglycemic agents and may affect lipid metabolism. Concentrations of cholesterol and triacylglycerols are of interest due to their association with diseases such as non-insulin-dependent-diabetes- mellitus and obese insulin resistance.
    METHODS AND RESULTS:
    As little is known about the effects of chlorogenic acid in vivo, studies using obese, hyperlipidemic, and insulin resistant (fa/fa) Zucker rats were conducted to test the effect of chlorogenic acid on fasting plasma glucose, plasma and liver triacylglycerols and cholesterol concentrations. Aditionally, the effects of chlorogenic acid on selected mineral concentrations in plasma, spleen, and liver were determined. Rats were implanted with jugular vein catheters. Chlorogenic acid was infused (5 mg/Kg body weight/day) for 3 weeks via intravenous infusion. Chlorogenic acid did not promote sustained hypoglycemia and significantly lowered the postprandial peak response to a glucose challenge when compared to the same group of rats before Chlorogenic acid treatment. In Chlorogenic acid-treated rats, fasting plasma cholesterol and triacylglycerols concentrations significantly decreased by 44% and 58% respectively, as did in liver triacylglycerols concentrations (24%). We did not find differences (p > 0.05) in adipose triacylglycerols concentration. Significant differences (p < 0.05) in the plasma, liver, and spleen concentration of selected minerals were found in chlorogenic acid-treated rats.
    CONCLUSIONS:
    In vivo, chlorogenic acid was found to improve glucose tolerance, decreased some plasma and liver lipids, and improve mineral pool distribution under the conditions of this study.
    Biomol Ther (Seoul) . 2014 Sep;22(5):420-5.
    Protective Effects of Chlorogenic Acid against Experimental Reflux Esophagitis in Rats[Pubmed: 25414772]
    Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-α, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.8224 mL 14.1119 mL 28.2239 mL 56.4477 mL 70.5597 mL
    5 mM 0.5645 mL 2.8224 mL 5.6448 mL 11.2895 mL 14.1119 mL
    10 mM 0.2822 mL 1.4112 mL 2.8224 mL 5.6448 mL 7.056 mL
    50 mM 0.0564 mL 0.2822 mL 0.5645 mL 1.129 mL 1.4112 mL
    100 mM 0.0282 mL 0.1411 mL 0.2822 mL 0.5645 mL 0.7056 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    新绿原酸; Neochlorogenic acid CFN97472 906-33-2 C16H18O9 = 354.3 20mg QQ客服:1457312923
    新绿原酸甲酯; Neochlorogenic acid methyl ester CFN95190 123410-65-1 C17H20O9 = 368.3 5mg QQ客服:1413575084
    5-O-阿魏酰奎尼酸; 5-O-Feruloylquinic acid CFN92889 40242-06-6 C17H20O9 = 368.3 10mg QQ客服:2159513211
    顺式5-O-阿魏酰奎尼酸; cis-5-O-Feruloylquinic acid CFN95659 87099-75-0 C17H20O9 = 368.3 10mg QQ客服:2056216494
    甲基 5-O-阿魏酰奎尼酸酯; Methyl 5-O-feruloylquinate CFN92445 154461-64-0 C18H22O9 = 382.4 5mg QQ客服:1457312923
    绿原酸; Chlorogenic acid CFN99116 327-97-9 C16H18O9 = 354.31 20mg QQ客服:215959384
    3-咖啡酰奎尼酸甲酯; 3-O-Caffeoylquinic acid methyl ester CFN92573 123483-19-2 C17H20O9 = 368.3 20mg QQ客服:2056216494
    绿原酸乙酯; Ethyl chlorogenate CFN91565 425408-42-0 C18H22O9 = 382.4 5mg QQ客服:2056216494
    3-O-阿魏酰奎尼酸; 3-O-Feruloylquinic acid CFN92393 1899-29-2 C17H20O9 = 368.3 5mg QQ客服:215959384
    甲基 3-O-阿魏酰奎尼酸酯; Methyl 3-O-feruloylquinate CFN92446 154418-15-2 C18H22O9 = 382.4 5mg QQ客服:2159513211

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